PATIENT ASSESSMENT ON ENDOCRINE SYSTEM.docx

ASSESSMENT
OF
ENDOCRINE SYSTEM
Submitted By:_
Komal
Roll No.:-402
NPCC 1st
year
Subject :- Advanced health assessment in critical
care nursing
Submitted To:-
Mrs. Rajpati
Lecturer
College of Nursing
Pt.B.D. Sharma PGIMS

I
PATIENT ASSESSMENT:- ENDOCRINE SYSTEM
Learning objectives :-
 History, physical examination, laboratory and diagnostic studies of
A. Hypothalamus and Pituitary Gland
B. Thyroid Gland
C. Parathyroid Gland
D. Endocrine Pancreas
E. Adrenal Gland

II
A. HYPOTHALAMUS AND PITUITARY GLAND
1. HISTORY TAKING
i. Demographic characteristics:- First A Nurse practitioner should introduce yourself to
patient , then ask:-
 Patient Name,
 Age
 Gender
 Hospital Id
 Occupation Address
 Date Of Admission (If Admitted)
 Education
ii. Chief complaints:- Ask the patient about the problem for which he or she came to the
hospital. Patient should describe their problem with either sign or symptom.
iii. History of present illness :- The nurse practitioner then ask the patient for more information
about presenting illness using the NOPQRST format. But most of the clinical sign and
symptoms that can occur in hypothalamus and pituitary disorders are:-
 excessive or inadequate urine output
 excessive thirst ,
 poor skin turgor ,
 cognitive changes
 dehydration
 water intoxication
NOPQRST Format is given below:-
 N Normal:- describe your normal baseline. What was it before symptom arised ?
 O Onset:- when did the symptom start ? what day? what time? did it start suddenly or
gradually?
 P Precipitating and Palliative factor:- What brought on symptoms ? What seems to trigger
it, factor such as stress, position change or exertion? What were you doing when you first
noticed the symptom? What makes the symptom worse? What measures have helped to
relieve the symptoms? What have you tried so far? What measures did not relieve the
symptoms?
 Q Quality and Quantity:- How does it feel? How would you describe it ? How much you are
experiencing now ? Is it more or less than you experienced at any other time?
 R Region and Radiation:- Where does the symptom occur, can you show me? In the case of
pain, if present, does it travel any where such as down your arm or back?

III
 S Severity:- How severe is the symptom occurred? Does it force you to stop your activity and
sit down ,lie down or slow down? Is the symptom getting better or worse or staying about
the same?
 T Time:- How long does the symptom last ?How often do you get the symptom ? Does it
occurs in association with anything such as before during or after meal?
iv. Past health history:- Ask the patient or relatives about past health history such as
 Relevant childhood illness and immunization:- history of adenoid or neck /chest radiation,
mental retardation, iodine deficiency
 Past acute and chronic medical problems:- diabetic emergency, hypertension ,high
cholesterol ,myocardial infarction, congestive heart failure, Graves disease, hashimoto
thyroiditis ,head injury ,cerebral vascular accident, pancreatitis and unexplained infection
 Risk factors:- age,hereditary, gender, race, tobacco use, alcohol use, elevated cholesterol,
obesity, sedentary lifestyle, pregnancy, gestational diabetes, delivery of an infant weighing
more than 9lb, anemia
 Past surgeries:- neurosurgical procedures, thyroidectory, parathyrodectomy, adrenectomy
 Medications:- amiodarone, phenytoin, carbamazepine, chlorpropramide corticosteroids,
Heparin, diuretics etc
 Allergy:- either related to medicines, food, contrast dye,latex or other material
 Transfusion history :-if any
v. Family History :- Is there any history of thyroid disease, diabetes, lipid disorders, Cancer,
aneurysms, autoimmune disorders in family members
vi. Personal & Social History:- Is there any history of tobacco , alcohol, substance abuse,
occupation , living environment: diet, excercing, sleep patterns
vii. Review of other systems
 HEENT:- headache, dizziness, weakness , visual changes
 Lymphatics:- edema, lymphadenopathy
 Genitourinary:- sexual dysfunction, infertility, abnormal vaginal delivery/Bleeding
2. PHYSICAL EXAMINATION
 Physical examination of the patient includes, assessment of hydration status, skin turger,
buccal membrane moisture, vital signs and weight are assessed.
 A patient with Hypovolemia would experience weight loss from excretion of large volume
of dilute urine.
 Eventually the patient would experience tachycardia, hypotension, poor skin turgor, dry
buccal membranes and cognitive changes associated with dehydration and hypernatremia.

IV
 Conversely a patient with Hypervolemia would display signs of water Intoxication, such as
edema, scant urinary output, weight gain, hypertension, moist buccal membranes, good skin
turgor and cognitive changes associated with Hyponatremia
 For patient experiencing fluid balance alterations, the nurse needs to maintain strict
measuring of intake and output. Urine specific gravity is measured routeinly, noting the
nature of urine.
 In addition, critically ill patients with fluid imbalance often have advanced monitoring
techniques in place such as central venous pressure or Hemodynamic monitoring with
pulmonary artery Catheter .Vigilant Monitoring of the patient's fluid status must be
maintained.
3. LABORATORY STUDIES :-
The following laboratory studies should be done while assessing Disorders of hypothalamus
and pituitary gland, are as given below:-
i) Serum Antidiuretic Hormone:-Normal Range:-1 to 13.3pg/ml.
This radioimmunoassay level distinguish between central diabetes Insipidus and SIADH.
Elevated serum ADH Compared with low serum osmolality and elevated urine osmolality
confirms the diagnosis of SIADH.
Reduced level of ADH correspondingly high serum osmolality, hypernatremia and reduced
urine concentration Indicates central diabetes insipidous.
ii) Urine specific Gravity: specific gravity reflect the kidney's ability to dilute and concentrate
urine. The range depends on hydration, urine volume and the amount of solids in urine.
LABORATO
RY
STUDIES
Antidiuretic Hormone
administration
Serum Antidiuretic
Hormone
Urine specific gravity
Serum osmolatily
Water deprivation Test
Urine osmolality

V
The specific gravity can be measured by using a multiple text dipstick that has a reagent for
specific gravity or by using a refrectometer .
Low specific gravity (1.001 to 1.010) is seen in diabetes insipidous and is accompanied by
copious, dilute urine.
Increased specific gravity (1.025 to 1.030) is seen in diabetes mellitus with dehydration , the
urine in general is more concentrated with smaller volumes.
iii) Serum Osmolality:- It ranges from 270 to 300 mOsm/kg and measures the concentrection
of diluted particles in the blood stream.
Elevated serum osmolality stimulates the release of ADH, which enhances the reabsorption
of fluid and sodium at the nephron Level. Through this process ECF volume is restored and
the plasma become less concentrated.
Hemodilution or decreased serum osmolality inhibits ADH, causing excess fluid to be
eliminated by the kidneys to maintain homeostasis.
Concentration of plasma is restored.
iv) Urine Osmolality: the test is a more exact measure of urine concentration. It is also a more
useful test when performed in conjuction with serum osmolality.
It can be used to diagnose kidney function, diabetes Insipidous, and psychogenic water
drinking.
The urine osmolality is increased in Addison disease,SIADH, dehydration and renal disease.
It is decreased in diabetes insipidous, and psychogenic water disease.
The normal range is 300 to 900 mOsm/kg/24 hr and 50 to 1200 mOsm/kg in a random sample
v) Water deprivation Test: - water restriction if a useful test, because healthy people respond
with a rapid decrease in urine volume when water intake is withheld.
People with diabetes insipidous have no decrease in urine volume in response to severe water
restriction. This signifies that normal mechanism of ADH release in the face of water
restriction and dehydration is dysfunctional.
This test is rarely performed in critical care unit because the patient is too ill and fragile to
withstand the rigors of severe dehydration .
The preferred test is measurement of serum ADH to diagnose diabetes insipidous
vi) ADH Administration: - It is one of the final test used to diagnose diabetes
insipidus .Exogenous ADH is given subcutaneously to the person suspected to have diabetes
Insipidus causes a temporary increase in urine osmolality.

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For a brief time, the person displays the appropriate respouse to ADH by conversing water
at the kidney level and urine output slows down in an attempt to restore ECF. This test also
help to distinguish b/w the two types of insipidous diabetes, nephrogenic & central.
In nephrogenic diabetes insipidous, the person doesn't not demonstrate a reaction to
exogenous ADH because the kidney receptors in collecting duct are unresponsive to ADH.
People with Central diabetes inspidus respond readily to the exogenous ADH.
4. DIAGNOSTIC STUDIES
 CT, MRI are essential in diagnosing primary diseases affecting this area of the brain .
 Examples of disorders affecting the pituitary Hypothalamic axis are Brain tumor, aneurysms,
edema from surgical exploration or traumatic injury and necrotic lesions.
 Imaging techniques are used to view the sella turcica and the surrounding structures including
the pituitary with in the bony encasement of the middle cranial fossa.
 Angiography assists with precise viewing of vascular supply in this area.
 Critical ill patients are required continuous monitoring at all times during these procedures.
Patient may get sedation also to eliminate movement to ensure clear imaging.
 CT is often used with contrast media to highlight specific areas of the brain and the patient
needs to be monitored for allergic reaction if sensitive to iodine, which may be contained in
the contrast agent.
 Institutional policies and procedures need to be followed during diagnostic testing.

VII
B. THYROID GLAND
1. HISTORY TAKING
i. Demographic characterctics:- First a nurse practitioner should introduce yourself to
patient.Then ask to patient
 Their Name
 Age
 Gender
 Hospital ID
 Occupation
 Address
 Date of admission (if admitted)
 Education
ii. Chief complaints: Ask the patient about the problem for
which he/she came to the hospital.
Patient should describe their Problem, either sign and symptoms.
iii. History of Present Illness:- The nurse practitioner then asks for more information about
presenting Illness, using NOPQRST format.
But most of the clinical sign and symptoms that Can occurs in thyroid disorders are:
 Cold or heat intolerance
 Edema
 Cognitive changes - such as slowed mentation, agitation, memory impairment and stupor
 Insomnia, fatigue, tachycardia, Atrial fibrilations Bradycardia, Hypoventilation,
constipation, diarrhoea
 Menstrual cycle irregularities.
 Skin problems, Husky voice diplopia , exophthalmos , eye pain, change in vision, depression,
Hematuria.
iv. Past Health History: Ask patient or relative about past health history
such as-
 Relevant childhood illness and immunization .
 Past acute and chronic medical problems:- diabetes emergency, Hypertension, high
Cholestrol, MI, CHF, Graves Disease,Hashimoto Thyroiditis, Head injury, CVA,
Pancreatitis, hypo/hyper thyroidism.
 Risk factors :- age, hereditary, gender, race, tobacco use, alcoholism, elevated cholesterol,
obesity, sedentary life style, Pregnancy

VIII
 Any H/o past surgeries
 Any medications that patient is taking.
 Any Allergy either to drugs or other factors
 Any Transfusion History.
v. Family History: Is there any History of Thyroid disorder in family like
Hypo/hyperthyroidism .
vi. Personal and Social History: Is there any History of tobacoo ,Alcohol substance Abuse.
What about patients occupation, living environment, diet, excercise, sleep patterns.
vii. Reviews of other systems:
HEENT - Headache, Dizziness , weakness, visual changes
Lymphatics:- Edema, lymphadenopathy
Genitourinary:- Sexual dysfunction, infertility, abnormal vaginal delivery/bleeding
Because of deep protect locations in the body, the endocrine glands are in general
inaccessible to do palpation, percussion and auscultation.
The exception is the thyroid gland, which can be inspected, palpated and could be auscultated
as well. So, let's discuss about all these steps.
1. INSPECTION:- Inspect the the anterior neck for assessment the area for enlargement,
nodule and symmetry of the gland. The patient is then asked to swallow while the nurse
practitioner observes the thyroid rising.
2. PALPATION:- Next the thyroid is palpated for size, shape, symmetry and presence of
tenderness . Thyromegaly (goiter) or thyroid nodules can be detected by palpation. Both lobes
of the gland and isthmus are palpated . Following are the steps for palpating the thyroid gland
STEPS:-
1. Ask the patient to flex the neck slightly forward to relax the sternomastoid muscles.
2. Place the finger of Both hands on the patients neck so that your index finger are Just below
the cricoid cartilage.
3. Ask the patient to sip and swallow water as before. Feel the thyroid isthmus rising up under
your finger pads. It is often but not always palpable.
4. Displace the trachea to the right with the fingers to the left hand then with the right hand
fingers ,palpate laterally for the right lobe of the thyroid in the space between the displaced

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Trachea and the relaxed sternomastoid find the lateral margin, In similar way, examine the
left lobe:
5. The lobes are somewhat harder to feel than the isthmus, so practice is needed.
6. The anterior surface of a lateral lobe is approximately the size of the distal phalanx of the
thumb and feels somewhat rubbery .
7. Note the size, shape and consistency of the gland and identify any nodule or tenderness.
8. If the thyroid is enlarged listen over the lateral lobes with a stethoscope to defect a bruit.
3. AUSCULTATION:- Occasionally, a thyroid bruit can be detected by listening over the
gland with the bell of the Stethoscope.
 A bruit is caused by excessive or turbulent blood flow associated with Hyperthyroidism and
the resultant hypermetabolic state.
 Other assessment parameters include noting vital sign changes, Skin changes (edema),
neurological changes and weight changes associated with either disorder.
 Hypothyroidism is frequently associated with Hypotension, Bradycardia ,
Hypoventilation ,Subnormal temprature.
 The patient often have: dry, flaky skin, edema over pretibial area ,deep or husky voice .
 The patient displayed slow cognitive functioning with slower than normal verbal responses.
 Hyperthyroidism is frequently associated with more neurological manifestations such as
Tremor, nervousness, insomnia and restless movements and Hyperactive reflexes.
 Characteristic vital signs are-
Hypertension, Tachycardia, Tachypnea, Hyperthermia.
 Patient may have goiter with detectable bruit.
 Patient Also may have exophthalmos or proptosis of the eyes socket, so that patient is unable
to close one or both eyes.
i. TSH
Test(Thyrotropin
Assay)
ii. Total
Thyroxine
iii. Free
Thyroxine & free
thyroxine index
v.Triiodothyronine
resin uptake test
iv. Free
triiodothyronine
viii.Thyroglobul
in
vii.Thyroid
antibodies
vi. Calcitonin

X
i. Thyroid stimulating hormone test
Or
Thyrotropin assay
 The TSH is a highly sensitive test used in diagnose Hypo/hyperthyroidism.
 The TSH test measures circulating TSH from the anterior pituitary.
 TSH stimulates the release and distribution of T3 and T4 stored in large amounts in thyroid
gland.
 Measuring TSH helps determine weather the hypothyroidism is primary (i.e caused by
dysfunction of the thyroid gland) or secondary (i.e caused by hypofunction of the anterior
pitutary).
 A high TSH level diagnose primary Hypothyroidism.
 The levels of TSH and free T4 are highly influenced by stress in critical ill patients .
 Malnutrition, Hepatic dysfunction, pregnancy and drugs affect TSH and free T4 level,
actual thyroid disease is not present. This is termed euthyroid sick syndrome.
 Therefore TSH Test results needs to be analyzed carefully.
 The normal adult value for TSH is 0.4 to 5.4 mIU/L.
ii. Total Thyroxine :-
The Total T4 test measures both the free T4 and the portion carried by thyroxine binding
globulin (TBG).
 T4 is increased in hyperthyroidism and decrease in hypothyroidism.
 The normal value in
Infants 9.8 to 22.6 mcg/dl
Childhood:- 5.6 to 166 mcg/dl
Adult:- 4.6 to 12 mcg/dl
Higher in pregnancy.
Lower in older adult because plasma proteins decrease as people age.
iii. Free Thyroxine And Free Thyroxine Index:
 Free T4 and free T4 index measure the free part of T4 , the part that is not bound to
Protein.
 Free T4 is the metabolically active form of the hormone that can be used by tissues.
 It makes up a small part of the total T4.
 The free T4 test is more useful than total T4 test in diagnosing hypofunction and
hyperfunction of the thyroid gland because it helps diagnose thyroid function when TBG
(Thyroxine Binding globulin) are abnormal.
 This test can also evaluate Thyroid replacement therapy.
 Radioisotopes can interfere with this test results and heparin can give false high readings.
 The test can be done by direct assay or by indirect measurements.

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 The direct assay normal value is 0.8 to 2.7 ng/ml.
 Free T4 index is 4.6 to 12 ng/ml.
iv. Free Triiodothyronine :- Free T3 measures the circulating T3 that exists in the free state
in blood unbound to protein..
 This is one measure to evaluate thyroid function.
 T3 is about 5 times more potent than T4. and is more metabolically active.
 Decreased value indicates Hypothyroidism.
 Radioisotopes also affects results.
 Normal adult value is 260 to 480pg/dl.
v. Triiodothyronine Resin uptake Test:- The T3 resin uptake test is an indirect measure of
TBG available to bind T3 and T4.
 It is increased with Thyrotoxicosis.
vi. Calcitonin:- Calcitonin or Thyrocalcitonin is a hormone secreted by the thyroid.
 It is secreted in response to high levels of calcium and reduces the calcium level by
increasing its deposition.
vii. Thyroid antibodies:- Severe autoimmune thyroid disease produce detectable antibodies.
 Specifically Graves disease, Hashimoto thyroiditis and chronic autoimmune thyroid disease
cause, elevations In antithyroid antibodies, detectable by Immunoassay techniques.
 These Conditions can lead to severe hypo/hyperthyroidism if not treated.
viii. Thyroglobulin:- Thyroglobulin can be measured by radioimmunoassay and is elevated in
most Thyroid disorders.
 This test has limited diagnostic value because it is nonspecific.
 It is used clinically to follow the progression of disease in a patient being treated for thyroid
cancer
4. DIAGNOSTIC STUDIES
There are various diagnostic studies given below
Thyroid scan and
Radio Active Iodine
uptake
Fine Needle biopsy Ultrasound

XII
a. Thyroid scan and radioactive iodine :-
 The radio iodine uptake test measures the rate of iodine uptake by the thyroid gland after
the administration of Iodine-123tracer (by capsule, solution, or IV injection).
 A scintillation counter then measure gamma rays released from The breakdown of the
tracer in the thyroid producing a visual representation of the radioactivity in the thyroid
gland, neck, and mediastinum.
 Scan time is about 20 minutes. Normally, the radioactive iodine is evenly distributed in the
thyroid gland and the scan shows a normal size, position and shape.
 The Thyroid scan may be performed in conjuction with a radioactive iodine uptake study.
After the patient takes the radioactive iodine, a count is made over the thyroid gland with a
scintillation counter at specific times.
 These nuclear test can indicate areas of increased and decreased function and provide data
to diagnose Hyper/hypothyroidism , nodules, ectopic thyroid tissue and cancer of thyroid.
b. Fine Needle Biopsy:- It is the diagnostic tool of choice for detecting malignancy for a
thyroid nodule .
 It is often the initial test for evaluation of any thyroid mass.
 The test is safe, quick and accurate and results are usually available with in hours to several
days.
c. Ultrasound:- Ultrasound of the thyroid gland uses high frequency sound waves to produce
an image of gland.
 It is an easy, non invasive procedure that has no radiation risks and can be performed at
bedside.
 The Test produces good images of structures and can detect masses, nodules, cysts and
enlargement of the gland.

XIII
C. PARATHYROID GLAND
Introduction
 The four parathyroid glands are located just posterior to thyroid gland and are sometime
damaged during thyroid surgeries.
 The parathyroid gland produces parathyroid hormone which maintain blood calcium and
phosphorus levels , neuromuscular activity, blood clotting function and the cell permeability.
1. HISTORY TAKING
i. Demographic characterctics:- First a nurse practitioner should introduce yourself to
patient, then ask to patient’s
 Name
 Age
 Gender
 Hospital ID
 Occupation
 Address
 Date of admission (if admitted)
 Education
ii. Chief complaints: Ask the patient about the problem for
which he/she came to the hospital.
Patient should describe their Problem, either sign and symptoms.
iii. History of Present Illness:- The nurse practitioner then asks for more information about
presenting Illness, using NOPQRST format. But most of the clinical sign and symptoms
that can occurs in parathyroid hormone disorders are :-
Apathy, Fatigue, weakness, tetany , joint pain and kidney stone pain.
iv. Past health history:- Ask patient or relative about past health history
such as-
 Past acute and chronic medical problems:- electrolyte imbalance specially related to calcium
and phosphorus

XIV
v. Family History: Is there any history of electrolyte imbalance specially related to calcium
and phosphorus in family.
 HEENT - Headache, Dizziness , weakness, visual changes
 Lymphatics:- Edema, lymphadenopathy
 Genitourinary:- Sexual dysfunction, infertility, abnormal vaginal delivery/bleeding
 Tetany can be assessed by evaluating the patient for trousseau sign and chvostek sign.
 Trousseau sign is positive when carpopedal spasm is induced by occluding the blood flow
to the arm for 3 minutes with the use of a blood pressure cuff.
 If tapping over the facial nerve just in front of the parotid gland causes twitching of the mouth
or eye, the patient has positive chvostek sign.
3. LABORATORY STUDIES
 Normal calcium level ranges from 8.6 to 10.3mg/dl.
 Most (99%) of body calcium is in the bone and remaining (1%) is in the extracellular fluid.
 Nearly 50% of serum calcium is ionized or free where is the remainder is bound to albumin.
 Marked serum calcium elevations (level greater than 10.3mg/dl) are the most obvious
manifestation of hyperparathyroidism.
 Common cause include primary hyperparathyroidism, malignancy, vitamin D toxicity,
hyperthyroidism and some medications such as thiazide diuretics and lithium.
 Low serum calcium levels are the marker for hypoparathyroidism.
 Tetany develops at calcium level of 5 to 6mg/dl or lower.
 Common causes of hypocalcemia include hypoalbuminemia, Renal failure,
hypoparathyroidism, acute pancreatitis, tumor lysis syndrome, severe hypomagnesemia and
multiple citrated blood transfusions.

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D. ENDOCRINE PANCREAS
1. HISTORY TAKING
 Patient Name,
 Age
 Gender
 Hospital Id
 Education
about presenting illness using the NOPQRST format. But most of the clinical sign and
symptoms that can occur in endocrine pancreatic disorders are:-
Weight gain or loss, excessive urination, excessive thirst, excessive appetite, blurred vision,
poor wound healing, dehydration etc.
such as-
 Past acute and chronic medical problems:- like diabetes mellitus.
v. Family History: Is there any history of diabetes mellitus in family .

XVI
 Physical examination focuses on the severe fluid and electrolyte and neurological
dysfunction seen with acute diabetes complications such as diabetic ketoacidosis, HHS and
hypoglycemia.
 Observation of fluid status and hydration is essential.
 Skin turger, buccal membranes , weight, urine specific gravity and vital signs are assessed.
 The nurse practitioner monitor patients neurological status frequently as well as Central
Venus pressure also
 Observe the presence of fruity order on the breath (associated with ketonemia) should be
noted.
 Assess kussmal respiration, the respiratory pattern is characterized by deep rapid breathing
1.
2.
3.
Fasting blood glucose
level and finger stick
glucose analysis
Glucagon
Insulin
Urine ketones
Serum ketones
Glycoslated
hemoglobin
(HbA1c)
C peptide level
Fructosamine

XVII
1. Fasting Blood Glucose Level and Fingerstick Glucose Analysis :- The fasting blood
glucose level provides a foundation for managing diabetes mellitus. Very high blood
glucose levels can occur in DKA and HHS.
 In addition, Hyperglycemia (elevated glucose levels) can occur in Cushing syndrome, high-
stress states, pancreatitis, and chronic renal and liver disease.
 Hypoglycemia can occur in Addison disease, pancreatic tumors, starvation, and
hypopituitary problems. The normal value for fasting glucose in adults is 65 to 110 mg/dl.
 Numerous drugs can interfere with glucose regulation, including corticosteroids, diuretics,
lithium, phenytoin, B-blockers, and estrogen. Hypoglycemic reactions can result from
sulfonylureas, insulin, alcohol, B-blockers, angiotensin- converting enzyme inhibitors, and
aspirin.
 Fingerstick glucose testing can be used at the bedside for immediate feedback regarding
the patient's glucose status. In addition, patients can be taught to use fingerstick devices at
home to monitor their glucose levels and responses to medi- cation. Standardization of the
equipment must be ensured when these devices are used for patient monitoring.
2. Glycosylated Hemoglobin:-
 Glycosylated hemoglobin (HbA1c) testing offers information about the average amount of
serum glucose that is bound to hemoglobin for the 100 to 120 day life span of erythrocytes.
 This information is now used to diagnose diabetes and to assess data trends for a person
who has been previously diagnosed with diabetes.
 The percentage result (normal: 4% to 7%) reflects an average of 3 months and enhances
accuracy because it controls for many variables such as stress, exercise, fasting state,
interfering medications, and recent changes in patient compliance.
3. Fructosamine:-
 Serum fructosamine level measures glycosylation of serum protein albumin.
 It is a useful index that reflects chronic glycemic control in patients with diabetes for whom
HbA1c may be inaccurate, such as those with anemia or hemoglobin abnormalities (eg,
sickle cell disease)."
4. Insulin:-
 An insulin test helps measure abnormal carbohydrate metabolism by measuring the amount
of circulating serum insulin in the fasting state.
 Abnormally high levels of insulin may help diagnose insulinoma, a tumor of the islets of
Langerhans.
 The normal adult value is 6 to 24 mcU/mL.
 A low insulin level helps diagnose diabetes mellitus, especially in the presence of an
abnormal GTT.
 Oral contraceptives and recent administration of radioisotopes interfere with results.

XVIII
5. C-Peptide Level:-
 C-peptide is a single chain of amino acids connecting A and B chains of insulin in the
proinsulin molecule. It has no known physiological function, but because it persists in
higher concentrations than insulin, it may be a more accurate reflection of insulin levels.
 It provides a useful monitor of average Beta-cell insulin secretion and can be used to
distinguish between types 1 and 2 diabetes mellitus.
 Normal values are some insulin 0.5 to 2.0 ng/mL and indicate that the body is still
producing some insulin. Low values (or no insulin C-peptide) indicate that the person's
pancreas is producing little or no insulin, as in type I diabetes.
6. Glucagon:-
 Glucagon, a hormone, produced in the alpha cells in the islets of Langerhans, controls the
production, storage, and release of glucose.
 Normally, insulin opposes the action of glucagon.
 The glucagon test measures the production and metabolism of glucagon.
 A deficiency occurs when pancreatic tissue is lost because of chronic pancreatitis or
pancreatic tumors.
 Increased levels occur in diabetes, acute pancreatitis, and catecholamine secretion (such as
occurs with infection, high stress levels, or pheochromocytoma).
 Chronic renal failure and cirrhosis of the liver can also increase glucagon levels.
 Normal fasting values are 50 to 200 pg/mL.
7. Serum Ketones:_
 Measuring serum ketones reveals information about the use of fat metabolism in lieu of
carbohydrates as seen in the critically ill person with diabetes.
 The normal serum ketone level is 2 to 4 mg/dL.
 Ketonemia (acetone, B-hydroxybutyrate, and acetoacetate) is manifested by Kussmaul
respirations and a fruity, sweet-smelling odor on the exhaled breath.
 These signs are the result of the patient's attempt to maintain a normal pH during extreme
metabolic acidosis.
 In DKA, metabolic acidosis is primarily the result of the accumulation of acetoacetic acid
and B-hydroxybutyric acid, the preferred method for estimating the severity of DKA.
8. Urine Ketones:-
 Ketones are not normally found in the urine. Ketones in the urine are associated with
diabetes and other diseases of altered carbohydrate metabolism.

XIX
 People with diabetes should test for ketones whenever their urine or blood glucose is high.
Because ketones appear in the urine before they can be detected in the blood, this test is
often used in the emergency department when screening for acidosis.
 The test is performed by dipping a ketone reagent strip in a fresh urine sample.
 The presence of ketones in the urine results from lipolysis or fat breakdown in the absence
of adequate insulin.

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E. ADRENAL GLAND
INTRODUCTION
 The adrenal gland is anatomically and functionally divided into two distinct parts:- The
outer cortex and the inner medulla .The two regions secrete different hormones.
 The cortex produces mineralocorticoids (eg, aldosterone), glucocorticoids (eg, cortisol),
and androgens.The medulla secretes catecholamines such as epinephrine, norepinephrine,
and dopamine.
 Disorders of the adrenal gland have widespread effects on the human body because these
hormones regulate major body functions, such as fluid and electrolyte balance, sympathetic
nervous system responses, inflammation, and metabolism.
 The secretion of hormones by the adrenal gland is regulated in a negative feedback system
through the hypothalamic-pituitary axis. The hypothalamus releases corticotropin-releasing
hormone, which in turn stimulates the release of ACTH from the anterior pituitary.ACTH
then stimulates the adrenal cortex to secrete cortisol.
1. HISTORY TAKING
 Patient Name,
 Age
 Gender
 Hospital Id
 Education
about presenting illness using the NOPQRST format. Most of the clinical manifestations of
adrenal gland dysfunction are sudden and severe headache, diaphoresis, palpitations, and
other symptoms associated with paroxysmal hypertension.
The resulting disease, Cushing syndrome, manifests as central obesity, unusual fat deposits,
thin extremities, fragile skin, skin discoloration (striae), sleep disturbances, and catabolism.

XXI
The resulting disease, Addison disease manifests as the patient becomes lethargic,
dehydrated, and unable to mount any stress response to handle acute illness or trauma
such as-
 Past acute and chronic medical problems:- like Cushing syndrome and Addison disease.
v. Family History: Is there any history of Cushing syndrome & Addison disease in family .
Physical examination of the patient includes, assessment of sudden and severe headache,
diaphoresis, palpitations, and other symptoms associated with paroxysmal hypertension.
The critically ill patient often suffers from mild forms of adrenal insufficiency because the
patient's normal stores of hormones are used quickly in response to the illness. Many
require exogenous steroids to assist with recovery.

XXII
So, observation is the only step in physical examination, because adrenal gland is not able
to palpitate, auscultate and not even get percussed by hands.
3. LABRATORY STUDIES
i. Cortisol (Hydrocortisone)
 The cortisol test evaluates the ability of the adrenal cortex to produce the glucocorticoid
hormone cortisol.
 Cortisol is elevated in adrenal hyperfunction and decreased in adrenal hypofunction.
 Adrenal hyperfunction may be caused by excess secretion of ACTH by the pituitary gland
(Cushing syndrome), high stress, trauma, and surgery.
 Adrenal hypofunction may be the result of anterior pituitary hyposecretion, hepatitis, and
cirrhosis.
Urine 17-Ketosteroids and
17-Hydroxycorticosteroids
Urine and Plasma
Catecholamine Levels
Cortisol
Stimulation
Cortisol
(Hydrocortisone)
Cortisol
(Dexamethas
one)
Suppression

XXIII
 Cortisol secretion is diurnal; it is normally higher in the early morning (6:00 AM to 8:00
AM) and lower in the evening (4:00 PM to 6:00 PM). This variation is lost in patients with
adrenal hyperfunction and in people under stress.
 Serum samples are drawn between 6:00 AM and 8:00 AM and between 4:00 PM and 6:00
PM.
 Normal 8:00 AM values are 5 to 23 fg/dL or 138 to 635 mmol/L.
 Normal 4:00 PM values are 3 to 16 fg/dL or 83 to 441 mmol/L.
ii. Cortisol (Dexamethasone) Suppression:- The cortisol suppression test is the test of
choice to diagnose Cushing syndrome.
 Before this test is started, medications are discontinued for 24 to 48 hours in particular,
estrogens, phenytoin, and cortisol-related preparations. Also, radioisotopes should not be
given within 1 week of this test.
 For this test, a low dose of dexamethasone (chemically similar to cortisol) is given at
bedtime.
 Blood samples are taken the next day at 8:00 AM and 4:00 PM. When healthy people
receive a low dose of dexamethasone, ACTH production is suppressed, but people with
adrenal hyperfunction and some with endogenous depression continue to produce ACTH
and do not have a diurnal variation of cortisol.
iii. Cortisol Stimulation:- Cortisol stimulation is the preferred test to diagnose Addison
disease.
 The cortisol stimulation test measures the response of the adrenal glands to an injection of
cosyntropin (Cortrosyn, a synthetic ACTH preparation).
 Blood is drawn for a fasting 8:00 AM cortisol level before cosyntropin is administered, and
then blood samples are taken 30 and 60 minutes after it is administered.
 The adrenal glands normally respond to the cosyntropin by synthesizing and secreting
adrenocorticoids. The plasma cortisol level should increase to at least 18 fg/dL.
 The response to cosyntropin is decreased or absent in people with adrenal insufficiency or
hypopituitarism.
 Long-term steroid therapy affects results.
 This test may be contraindicated in the presence of infections, inflammatory diseases, and
cardiac disease.
iv. Urine and Plasma Catecholamine Levels:-
 Urine vanillylmandelic acid, a metabolite of catecholamines, is rarely used diagnostically
today.

XXIV
 It is preferred to measure free and fractionated plasma metanephrines, fractionated and total
urine metanephrines, and plasma normetanephrines, because they yield higher sensitivity
levels for pheochromocytoma.
 Since metanephrines have high concentration in the urine and are easy to detect, a 24-hour
urine test is performed when a person is suspected of having hypertension due to
pheochromocytoma.
 Elevated levels of catecholamines can be found in patients with hypothyroidism, DKA,
neuroblastomas, and ganglioneuromas.
 Urine should not be collected when the patient is fasting. Test results are also affected by
many drugs and foods, such as tea, coffee, vanilla, and fruit juice.
 Therefore, some laboratories restrict certain foods for 2 days before testing and on the day
of testing. Certain drugs may also be discontinued for 4 to 7 days before testing.
 Normal adult value for urine catecholamines is 270 fg/24 hr.
v. Urine 17-Ketosteroids and 17-Hydroxycorticosteroids:- Adrenal function can be tested
by measuring the urinary excretion of steroids. These 24-hour urine collection tests are used
infrequently because they have been replaced by serum immunoassays.
4. DIAGNOSTIC STUDY
i. Adrenal scan:- An adrenal scan is used to identify the site of certain tumors or sites that
produce excessive amounts of catecholamines.
 The radionuclide iobenguane (131
I) is injected intravenously and scans are performed on
days 2, 3, and 4.
 In some patients the tumor or site of excessive catecholamine production can be identified
on day 2, whereas in other patients additional imaging is needed on days 6 and 7.
 Typically, no tumor or site of hypersecretion is found. If ACTH levels are elevated, MRI of
the pituitary should be done to seek the source.

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